Different HLA class I‐specific killer inhibitory receptors (KIR) are expressed in vivo by a fraction of activated T cells, predominantly CD8⁺ , in which they may inhibit TCR‐mediated cell functions. In an attempt to identify mechanisms leading to KIR expression in T cells, we analyzed the effect of transforming growth factor‐β (TGF‐β) in T cells responding to bacterial superantigens in vitro. We show that TGF‐β induces the expression of CD94/NKG2A in cells responding to toxic shock syndrome toxin 1 or to other staphylococcal superantigens. Remarkably, maximal CD94 expression occurred at (low) TGF‐β concentrations which have no substantial effect on lymphocyte proliferation. Maximal CD94 expression occurred when TGF‐β was added shortly after the cells were placed in culture. No expression could be induced in CD94/NKG2A‐negative T cell clones. Although both CD4⁺ and CD8⁺ expressed CD94, the simultaneous expression of NKG2A was mostly confined to CD8⁺ cells. Monoclonal antibody‐mediated cross‐linking of CD94/NKG2A led to an impairment of T cell trigger ing via CD3, as determined in a redirected killing assay using the Fcγ receptor‐positive P815 murine target cells.